13. Dynamic hyperinflation/ intrinsic PEEP predispositions Small airway inflammation/ secretions/ collapse High respiratory rate Short expiratory time Large I:E ratio Patient/ ventilator asynchrony and breath stacking
14. Effects of dynamic hyperinflation ↑ end expiratory volume ↓tidal volume, with tidal ventilation occurring near total lung capacity ↓venous return and compromised cardiac output-> hemodynamic collapse and arrest Inspiratory muscles placed at a mechanical disadvantage- inefficient force/length relationship Increased risk of barotrauma, non-cardiogenicedema, pneumothorax Increased pulmonary hypertension, increased RV load
15. Elevated V/Q ratio Areas of V/Q of 10-40 in acute small airway disease Normal V/Q=1.0
22. Additional therapies Pre-emptive pleural catheter in the face of high airway pressures and risk of alveolar rupture/ tension pneumothorax Continuous tracheal insufflation of O2 via catheter positioned at carina- increased deadspace washout of CO2 Sodium bicarbonate low 0.5mEq/kg dose
23. Respiratory acidosis- NaHCO3 ? Positives Protective against increased cerebral blood flow and ICP elevations associated with hypercapnic acidosis post anoxic brain injury May relieve severe pulmonary hypertension exacerbated by hypercapnic acidosis mediated pulmonary vasoconstriction Treats decreased contractility of cardiac and vascular muscle ?
24. Negatives Effectiveness depends on ability to eliminate CO2 May raise PaCO2 in the context of hypoventilation May correct arterial pH but worsen intracellular acidosis Removal of the acidosis-mediated protective effects of hypercapnia on the cardiovascular system Extracellular pH may not reflect intracellular
25. Effects of hypercapnic acidosis Augmentation of pulmonary hypoxic vasoconstriction, reducing shunt Increased lung compliance -surfactant Protective against pulmonary ischemia/ reperfusion injury Facilitation of O2 unloading to tissues via Bohr effect on Hb dissociation curve Elevated cardiac output mediated through endogenous catecholamine release, same effect reduces GFR and increases renal fluid retention Increased cerebral tissue, intestinal wall and renal PO2 Protective vs cell death in anoxic hepatocytes
26. Monitoring of ventilation PaO2/ FiO2 ratio <200 ARDS, <300 ALI Oxygen Index Pmean%O2 ------------------------- PaO2 normal <2.0 Dead space fraction VD/VT=(PaCO2-PECO2)/PaCO2 Rapid shallow index f/VT<105 without mechanical support via ET tube
28. Overview of eosinophilicbronchopneumopathy Aetiology uncertain, suspected hypersensitivity to aerosolized antigens Increased CD4+:CD8+ T cell ratio ↑MMP activity -> collagenolysis/proteolysis with airway destruction/remodeling ↑eosinophil specific chemokines Gender bias towards females
29. Average age at presentation 4-6 years (range 3mths-13yrs) Cough +/- nasal discharge Diagnosis on BALF cytology R/O heartworm dx R/O helminth trigger vsfenbendazole trial Oral/inhaled glucocorticoids- avoid abrupt discontinuation/ parenteral depots Start @ 1mg/kg prednisone bid and taper after one to 2 weeks
30. Outcome for Mr Magoo Successfully weaned from mechanical ventilation after 60 hours of support 48 hrs later Nasal O2 support d/c Pneumothorax resolved and pleural catheter removed Left forelimb lameness
31. Suprascapular neuropathy Marked atrophy supraspinatus + infraspinatus m. Radial n reflex and proprioception intact Weak withdrawal Suspected critical illness polyneuropathy
Artificially ventilated on 80% oxygen for approx 40 min. Partial compensation implies degree of chronicity- renal bicarb retention typically takes 48 hours to have a significant effect
80% eosinophils and erythrophagia, airway hemorrhage, erthrophagia implies hemorrhage of several hours duration ie not iatrogenic
Key to understanding pathology of small airway disease. Results from effects of small airway collapse during EXPIRATION. Equivalent to breathing in normally, and then trying to breath out through a straw. Effect of this is worse at elevated resp rates e-g during exercise, hypoxia, hypercarbia, anything causing a high respiratory drive. Due to the difficulty of eliminating sufficient volume during the available expiratory time, successive breaths start to volume stack on each other. (Discuss graph and pictures) This continues until lung volume is so high that the elevated elastic recoil pressure together with the increased airway diameter is able to increase expiratory flow.
Particularly difficult in the context of mechanical ventilation as not easy to correct/ detect. Inspiratory muscle length/ contraction relationship distorted.
Rate reduction difficult in context of hypercapnia
Tobin p378 but overall effects on CVS negative as blocks CO2 associated catecholamine release
P375 tobin
Fundamental dichotomy is when to intervene and treat low pH, and what with. Complete shift away from corrections to normal, and relative shift away from correction at all, current recommendations are to correct no higher than a pH of 7.1 in this context. Increasing case reports of patient survival with no ill efects at pH levels of 6.5-6.7. Relative indications to treat are clinical suspicion of hemodynamic instability resulting from direct myocardial depression effect.
Dead space fraction = anatomic AND physiologic
Good prognosis re response to therapy.
2 weeks later
Numerous obvious parallels. Mr Magoo returned to normal with recovery of muscle mass 3 months later. Currently doing well, steroids tapered to 0.5mg/kg once daily.